Literature DB >> 21757867

Truncated peroxisome proliferator-activated receptor-γ coactivator 1α splice variant is severely altered in Huntington's disease.

Ashu Johri1, Anatoly A Starkov, Abhishek Chandra, Thomas Hennessey, Abhijeet Sharma, Sara Orobello, Ferdinando Squitieri, Lichuan Yang, M Flint Beal.   

Abstract

BACKGROUND: Reduced peroxisome proliferator-activated receptor-γ coactivator 1α (PGC1α) gene expression has been observed in striatal cell lines, transgenic mouse models of Huntington's disease (HD), and brain tissue from HD patients. As this protein is a key transcription regulator of the expression of many mitochondrial proteins, these observations strongly support the role of aberrant mitochondrial function in the pathogenesis of HD. The PGC1α protein undergoes posttranslational modifications that affect its transcriptional activity. The N-truncated splice variant of PGC1α (NT-PGC1α) is produced in tissues, but the role of truncated splice variants of PGC1α in HD and in the regulation of mitochondrial gene expression has not been elucidated.
OBJECTIVE: To examine the expression and modulation of expression of NT-PGC1α levels in HD. METHODS AND
RESULTS: We found that the NT-PGC1α protein, a splice variant of ∼38 kDa, but not full-length PGC1α is severely and consistently altered in human HD brain, human HD myoblasts, mouse HD models, and HD striatal cells. NT-PGC1α levels were significantly upregulated in HD cells and mouse brown fat by physiologically relevant stimuli that are known to upregulate PGC1α gene expression. This resulted in an increase in mitochondrial gene expression and cytochrome c content.
CONCLUSION: Our data suggest that NT-PGC1α is an important component of the PGC1α transcriptional network, which plays a significant role in the pathogenesis of HD.
Copyright © 2011 S. Karger AG, Basel.

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Year:  2011        PMID: 21757867      PMCID: PMC3186722          DOI: 10.1159/000327910

Source DB:  PubMed          Journal:  Neurodegener Dis        ISSN: 1660-2854            Impact factor:   2.977


  27 in total

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Review 2.  Huntington disease.

Authors:  J P Vonsattel; M DiFiglia
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Authors:  L Mangiarini; K Sathasivam; M Seller; B Cozens; A Harper; C Hetherington; M Lawton; Y Trottier; H Lehrach; S W Davies; G P Bates
Journal:  Cell       Date:  1996-11-01       Impact factor: 41.582

4.  Specific progressive cAMP reduction implicates energy deficit in presymptomatic Huntington's disease knock-in mice.

Authors:  Silvia Gines; Ihn Sik Seong; Elisa Fossale; Elena Ivanova; Flavia Trettel; James F Gusella; Vanessa C Wheeler; Francesca Persichetti; Marcy E MacDonald
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Review 5.  Transcriptional abnormalities in Huntington disease.

Authors:  Katharine L Sugars; David C Rubinsztein
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6.  Defects in adaptive energy metabolism with CNS-linked hyperactivity in PGC-1alpha null mice.

Authors:  Jiandie Lin; Pei-Hsuan Wu; Paul T Tarr; Katrin S Lindenberg; Julie St-Pierre; Chen-Yu Zhang; Vamsi K Mootha; Sibylle Jäger; Claudia R Vianna; Richard M Reznick; Libin Cui; Monia Manieri; Mi X Donovan; Zhidan Wu; Marcus P Cooper; Melina C Fan; Lindsay M Rohas; Ann Marie Zavacki; Saverio Cinti; Gerald I Shulman; Bradford B Lowell; Dimitri Krainc; Bruce M Spiegelman
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7.  Intranuclear inclusions and neuritic aggregates in transgenic mice expressing a mutant N-terminal fragment of huntingtin.

Authors:  G Schilling; M W Becher; A H Sharp; H A Jinnah; K Duan; J A Kotzuk; H H Slunt; T Ratovitski; J K Cooper; N A Jenkins; N G Copeland; D L Price; C A Ross; D R Borchelt
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8.  Decreased cAMP response element-mediated transcription: an early event in exon 1 and full-length cell models of Huntington's disease that contributes to polyglutamine pathogenesis.

Authors:  Katharine L Sugars; Rosemary Brown; Lynnette J Cook; Jina Swartz; David C Rubinsztein
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10.  Dominant phenotypes produced by the HD mutation in STHdh(Q111) striatal cells.

Authors:  F Trettel; D Rigamonti; P Hilditch-Maguire; V C Wheeler; A H Sharp; F Persichetti; E Cattaneo; M E MacDonald
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3.  Potential roles of PINK1 for increased PGC-1α-mediated mitochondrial fatty acid oxidation and their associations with Alzheimer disease and diabetes.

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4.  mRNA expression levels of PGC-1α in a transgenic and a toxin model of Huntington's disease.

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Review 5.  Thermodynamics in Neurodegenerative Diseases: Interplay Between Canonical WNT/Beta-Catenin Pathway-PPAR Gamma, Energy Metabolism and Circadian Rhythms.

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Review 6.  Mitochondrial dysfunction in neurodegenerative diseases.

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7.  Pharmacologic activation of mitochondrial biogenesis exerts widespread beneficial effects in a transgenic mouse model of Huntington's disease.

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Review 9.  PGC-1α, mitochondrial dysfunction, and Huntington's disease.

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10.  Enhanced mitochondrial biogenesis ameliorates disease phenotype in a full-length mouse model of Huntington's disease.

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